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        心肌運(yùn)動(dòng)定量技術(shù)在多囊卵巢合并胰島素抵抗患者左室縱向心肌功能評(píng)價(jià)中的價(jià)值

        2018-11-10 10:02:36杜啟亙米香琴徐宏偉商瑋珉周立平陳巍
        中國醫(yī)藥導(dǎo)報(bào) 2018年19期

        杜啟亙 米香琴 徐宏偉 商瑋珉 周立平 陳巍

        [摘要] 目的 探討心肌運(yùn)動(dòng)定量(CMQ)技術(shù)評(píng)價(jià)多囊卵巢合并胰島素抵抗(PCOS-IR)患者左心室縱向運(yùn)動(dòng)的臨床價(jià)值。 方法 選取2016年2月~2017年2月在黑龍江中醫(yī)藥大學(xué)附屬第二醫(yī)院婦科就診的PCOS-IR患者55例為PCOS-IR組,另選擇年齡相匹配的55名健康婦女為對(duì)照組。記錄一般資料:腰臀比(WHR)、體重指數(shù)(BMI)、收縮壓(SBP)、舒張壓(DBP)、三酰甘油(TG)、高密度脂蛋白膽固醇(HDL-C)、低密度脂蛋白膽固醇(LDL-C)、空腹血糖(FPG)、空腹血漿胰島素(FINS)、胰島素抵抗指數(shù)(HOMA-IR),進(jìn)行常規(guī)超聲心動(dòng)圖檢查,測量左室舒張末期內(nèi)徑(LVDd)、左室收縮末期內(nèi)徑(LVDs)、舒張末期室間隔厚度(IVSTd)、舒張末期左室后壁厚度(LVPWTd)、左室射血分?jǐn)?shù)(LVEF)、舒張?jiān)缙诙獍昕谘鞣逯邓俣龋‥)、舒張晚期二尖瓣口血流峰值速度(A)、舒張?jiān)缙诙獍戥h(huán)運(yùn)動(dòng)峰值速度(Em),計(jì)算E/A及E/Em,測量E峰減速時(shí)間(DT)、等容舒張時(shí)間(IVRT)及等容收縮時(shí)間(IVCT)。應(yīng)用CMQ技術(shù)跟蹤描記心肌運(yùn)動(dòng)軌跡,獲取左室18節(jié)段心肌收縮期縱向峰值應(yīng)變(LS)及收縮期整體縱向峰值應(yīng)變(GLS)。采用Pearson相關(guān)分析各參數(shù)之間的相關(guān)性。 結(jié)果 PCOS-IR組WHR、BMI、FINS、HOMA-IR、LDL-C高于對(duì)照組,差異有統(tǒng)計(jì)學(xué)意義(P < 0.05)。兩組年齡、SBP、DBP、FPG、HDL-C、TG比較,差異無統(tǒng)計(jì)學(xué)意義(P > 0.05)。與對(duì)照組比較,PCOS-IR組DT、IVRT、E/Em增加,Em減小,差異有統(tǒng)計(jì)學(xué)意義(P < 0.05);兩組LVDd、LVDs、IVSTd、LVPWTd、LVEF、E、A、E/A、IVCT比較,差異無統(tǒng)計(jì)學(xué)意義(P > 0.05)。PCOS-IR組各節(jié)段LS及GLS均較對(duì)照組減低,差異有統(tǒng)計(jì)學(xué)意義(P < 0.05)。GLS與FINS、WHR及LDL-C均呈負(fù)相關(guān)(r = -0.58、-0.46、-0.44,P < 0.05),與FPG、HOMA-IR、HDL-C、TG、BMI無相關(guān)性(P > 0.05)。 結(jié)論 PCOS-IR患者在LVEF正常情況下可出現(xiàn)早期縱向收縮功能下降。CMQ技術(shù)可早期檢測出PCOS-IR患者左心室縱向運(yùn)動(dòng)異常,為臨床及時(shí)干預(yù)治療提供幫助。

        [關(guān)鍵詞] 多囊卵巢;胰島素抵抗;心肌運(yùn)動(dòng)定量技術(shù);左心室

        [中圖分類號(hào)] R711.75 [文獻(xiàn)標(biāo)識(shí)碼] A [文章編號(hào)] 1673-7210(2018)07(a)-0071-05

        Evaluation of left ventricular longitudinal myocardial function in patients with polycystic ovary syndrome associated with insulin resistance by cardiac motion quantification

        DU Qigen MI Xiangqin XU Hongwei SHANG Weimin ZHOU Liping CHEN Wei

        Department of Ultrasound, Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Heilongjiang Province, Harbin 150000, China

        [Abstract] Objective To investigate the clinical value of myocardial motion quantification (CMQ) in evaluation of left ventricular longitudinal motion in patients with polycystic ovary combined with insulin resistance (PCOS-IR). Methods From the February 2016 to February 2017, 55 patients with PCOS-IR in Department of Gynecology, the Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine were selected, 55 age matched healthy women were selected as control group. The general data were recorded: waist-to-hipratio (WHR), body mass index (BMI), systolic pressure (SBP), diastolic pressure (DBP), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), fasting blood glucose (FPG), fasting plasma insulin (FINS), homeostasis model assessment for IR index (HOMA-IR), and all subjects were given routine echocardiography, the left ventricular end-diastolic dimension (LVDd) and left ventricular end-systolic diameter (LVDs), end-diastolic interventricular septum thickness (IVSTd), end-diastolic left ventricular posterior wall thickness (LVPWTd), and left ventricular ejection fractional (LVEF), early diastolic blood flow peak velocity (E), late diastolic blood flow peak velocity (A), mitral annular early diastolic motion peak velocity (Em) were measured, E/A and E/Em were calculated, E peak deceleration time (DT), isovolumic relaxation time (IVRT) and isovolumic contraction time (IVCT) were measured. CMQ technique was used to trace tracing of myocardial trajectory, and systolic longitudinal peak strain (LS) and systolic global longitudinal peak strain (GLS) of 18 left ventricular segments were obtained. Pearson correlation was used to analyze the correlation between the parameters. Results The WHR, BMI, FINS, HOMA-IR and LDL-C in the PCOS-IR group were higher than those in the control group, the differences were statistically significant (P < 0.05); there was no significant difference in age, SBP, DBP, FPG, HDL-C, TG between the two groups (P > 0.05). Compared with the control group, DT, IVRT, E/Em increased in the PCOS-IR group, and Em decreased, the differences were statistically significant (P < 0.05); there was no significant difference in LVDd, LVDs, IVSTd, LVPWTd, LVEF, E, A, E/A, IVCT between the two groups (P > 0.05). The LS and GLS in each segment of PCOS-IR group were lower than those in the control group, the differences were statistically significant (P < 0.05). There were negative correlations between GLS and FINS, WHR, LDL-C (r = -0.58, -0.46, -0.44, all P < 0.05). There was no correlation between GLS and FPG, HOMA-IR, HDL-C, TG, BMI (P > 0.05). Conclusion Patients with PCOS-IR may show a decline in early longitudinal systolic function under normal LVEF. CMQ technology can detect early left ventricular longitudinal movement abnormalities in patients with PCOS-IR, and provide clinical help for timely intervention.

        [Key words] Polycystic ovary; Insulin resistance; Quantitative myocardial motion; Left ventricle

        多囊卵巢綜合征(PCOS)以稀發(fā)排卵和高雄激素血癥為特點(diǎn),在育齡婦女中發(fā)病比例高且多伴有胰島素抵抗(IR)[1-2],罹患心血管疾?。–VD)的風(fēng)險(xiǎn)升高[3]。本研究目的為應(yīng)用心肌運(yùn)動(dòng)定量(CMQ)技術(shù)定量評(píng)估PCOS-IR患者左心室縱向心肌運(yùn)動(dòng),探討PCOS-IR患者心肌局部及整體收縮功能,該方法能夠在常規(guī)二維超聲心動(dòng)圖未發(fā)現(xiàn)射血分?jǐn)?shù)(LVEF)降低之前,早期發(fā)現(xiàn)左心室局部心肌功能障礙,對(duì)臨床早期干預(yù)及治療有著重要意義。

        1 資料與方法

        1.1 一般資料

        選擇2016年2月~2017年2月黑龍江中醫(yī)藥大學(xué)附屬第二醫(yī)院(以下簡稱“我院”)婦科就診的PCOS-IR患者55例,患者年齡26~39歲,平均(30.13±5.26)歲,均符合2003年Rotterdam會(huì)議制訂的PCOS診斷標(biāo)準(zhǔn)[4],以穩(wěn)態(tài)模型評(píng)估的胰島素抵抗指數(shù)(HOMA-IR)≥1.66為IR。HOMA-IR=FINS(空腹胰島素)×FPG(空腹血漿血糖)/22.5[5]。剔除其他內(nèi)分泌疾病如甲狀腺功能亢進(jìn)、庫欣綜合征、先天性腎上腺皮質(zhì)增生等。另選取同期我院體檢的年齡匹配的健康女性55例為對(duì)照組,年齡25~40歲,平均(29.47±6.32)歲,月經(jīng)規(guī)律,超聲顯示雙側(cè)卵巢形態(tài)正常。兩組均排除吸煙、酗酒、糖尿病、近6個(gè)月內(nèi)妊娠或使用避孕藥物、近6個(gè)月內(nèi)有血栓或栓塞史者。本研究經(jīng)醫(yī)院醫(yī)學(xué)倫理委員會(huì)批準(zhǔn),所有研究對(duì)象均知情同意并簽署知情同意書。

        1.2 觀察指標(biāo)及檢測方法

        選用飛利浦IU-22彩色多普勒超聲診斷儀,S5-1心臟探頭,頻率1~5 MHz,幀頻≥60幀/s,儀器內(nèi)置QLAB分析軟件。

        1.2.1 記錄受試對(duì)象一般資料 腰臀比(WHR)、體重指數(shù)(BMI)、收縮壓(SBP)、舒張壓(DBP)、三酰甘油(TG)、高密度脂蛋白膽固醇(HDL-C)、低密度脂蛋白膽固醇(LDL-C)、空腹血糖(FPG)、空腹血漿胰島素(FINS)、胰島素抵抗指數(shù)(HOMA-IR)。

        1.2.2 心臟超聲評(píng)價(jià) 心臟超聲檢查:受檢者取左側(cè)臥位,平靜呼吸,連接心電監(jiān)測。行常規(guī)二維超聲心動(dòng)圖檢查,于胸骨左緣第2~4肋間獲取左室長軸切面,測量左室舒張末期內(nèi)徑(LVDd)、左室收縮末期內(nèi)徑(LVDs)、舒張末期室間隔厚度(IVSTd)及舒張末期左室后壁厚度(LVPWTd),采用雙平面Simpson法計(jì)算左室射血分?jǐn)?shù)(LVEF)。于心尖四腔心切面測量二尖瓣口舒張?jiān)缙谘鞣逯邓俣龋‥),舒張晚期血流峰值速度(A),并計(jì)算E/A;放置TDI取樣容積于二尖瓣環(huán),在室間隔及側(cè)壁兩個(gè)部位測量取平均值,測量舒張?jiān)缙诙獍戥h(huán)峰值運(yùn)動(dòng)速度(Em),并計(jì)算E/Em,測量E峰減速時(shí)間(DT)、等容舒張時(shí)間(IVRT)及等容收縮時(shí)間(IVCT)。

        1.2.3 CMQ技術(shù)對(duì)左心室縱向心肌運(yùn)動(dòng)的評(píng)價(jià) 采集并儲(chǔ)存連續(xù)3個(gè)心動(dòng)周期的左室心尖長軸四腔心切面、三腔心切面和兩腔心切面的二維超聲動(dòng)態(tài)圖像,將儲(chǔ)存圖像導(dǎo)入QLAB工作站中的CMQ模式進(jìn)行分析,選取清晰圖像,借助軟件標(biāo)記點(diǎn)勾畫左心室心內(nèi)膜及心外膜邊界,軟件自動(dòng)將左室壁分為6個(gè)節(jié)段,追蹤描記18節(jié)段各節(jié)段心肌斑點(diǎn)的運(yùn)動(dòng),生成左室節(jié)段心肌的收縮期應(yīng)變曲線,獲取各節(jié)段收縮期峰值縱向應(yīng)變(LS)及整體縱向應(yīng)變(GLS)。

        1.3 統(tǒng)計(jì)學(xué)方法

        采用統(tǒng)計(jì)軟件SPSS 20.0對(duì)數(shù)據(jù)進(jìn)行分析,正態(tài)分布的計(jì)量資料以均數(shù)±標(biāo)準(zhǔn)差(x±s)表示,兩組間比較采用t檢驗(yàn);計(jì)數(shù)資料以率表示,采用χ2檢驗(yàn)。參數(shù)間相關(guān)性分析采用Pearson相關(guān)分析。以P < 0.05為差異有統(tǒng)計(jì)學(xué)意義。

        2 結(jié)果

        2.1 兩組一般臨床參數(shù)比較

        PCOS-IR組WHR、BMI、FINS、HOMA-IR、LDL-C高于對(duì)照組,差異有統(tǒng)計(jì)學(xué)意義(P < 0.05)。PCOS-IR組年齡、SBP、DBP、FPG、HDL-C、TG與對(duì)照組比較,差異無統(tǒng)計(jì)學(xué)意義(P > 0.05)。見表1。

        2.2 兩組常規(guī)超聲心動(dòng)圖參數(shù)比較

        與對(duì)照組比較,PCOS-IR組DT、IVRT、E/Em增加,Em減小,差異有統(tǒng)計(jì)學(xué)意義(P < 0.05);PCOS-IR組LVDd、LVDs、IVSTd、LVPWTd、LVEF、E、A、E/A、IVCT與對(duì)照組比較,差異無統(tǒng)計(jì)學(xué)意義(P > 0.05)。見表2。

        2.3 左心室各節(jié)段心肌LS及GLS比較

        PCOS-IR組GLS(-15.39±1.58)與對(duì)照組(-17.74±2.03)比較,差異有統(tǒng)計(jì)學(xué)意義(P < 0.05)。PCOS-IR組各節(jié)段LS較對(duì)照組減低,差異均有統(tǒng)計(jì)學(xué)意義(P < 0.05)。見表3。

        2.4 心肌GLS與常規(guī)臨床指標(biāo)的相關(guān)性分析

        GLS與FINS、WHR及LDL-C呈負(fù)相關(guān)(r = -0.58、-0.46、-0.44,P < 0.05),與FPG、HOMA-IR、HDL-C、TG、BMI無相關(guān)性(P > 0.05)。見表4。

        3 討論

        PCOS以慢性無排卵、高雄激素血癥及多毛癥為特征,是育齡期婦女常見的內(nèi)分泌疾病[1-2]。PCOS患者極易罹患心血管疾病,有報(bào)道稱PCOS患者心肌梗死發(fā)生率是正常人的7倍[3],冠狀動(dòng)脈硬化發(fā)生率遠(yuǎn)高于正常排卵女性[6]。PCOS患者多合并IR,IR是PCOS患者心血管疾病的重要危險(xiǎn)因素[7]。PCOS患者出現(xiàn)亞臨床左室收縮功能障礙呈現(xiàn)年輕化[8],因此檢測左室縱向收縮功能異常對(duì)于降低PCOS患者心血管疾病發(fā)病率和死亡率有重要意義。CMQ技術(shù)是近年來無創(chuàng)定量評(píng)價(jià)左室心肌力學(xué)的新技術(shù),它基于斑點(diǎn)追蹤技術(shù),可以追蹤心內(nèi)膜、心外膜及整體室壁的運(yùn)動(dòng),從縱向、徑向及圓周方向全方位評(píng)估不同區(qū)域心肌運(yùn)動(dòng),可準(zhǔn)確、定量評(píng)估局部及整體心肌功能。

        以往研究證實(shí)PCOS患者多伴有心血管異常,包括:心臟收縮期峰值血流速度降低、舒張功能障礙、大動(dòng)脈僵硬度增加,血管內(nèi)皮功能障礙等[9-11]。本研究結(jié)果顯示,PCOS-IR患者DT、IVRT、E/Em增加,Em減小,提示PCOS-IR患者早期心肌損害主要表現(xiàn)為左室舒張功能減低。原因可能為PCOS患者多伴有冠狀動(dòng)脈疾病、血脂異常、血管內(nèi)皮功能障礙、輕度炎癥和氧化應(yīng)激[12-14],導(dǎo)致心肌細(xì)胞缺氧、纖維化。IR也可能是PCOS患者左室舒張功能減低的主要危險(xiǎn)因素[15]。TlRA等[16]研究發(fā)現(xiàn)IR與左室舒張功能呈顯著負(fù)相關(guān)。

        心肌具有復(fù)雜的解剖結(jié)構(gòu)以及復(fù)雜的運(yùn)動(dòng)形式,心肌收縮時(shí)產(chǎn)生沿長軸及短軸的運(yùn)動(dòng)[17]。左室長軸縱向運(yùn)動(dòng)在心臟力學(xué)中起重要作用,其機(jī)制為:收縮期左室縱向心肌將二尖瓣環(huán)向心尖部拉近,在長軸方向縮小左室容積,有助于心室射血[18-19];舒張?jiān)缙诳v向心肌釋放在收縮期儲(chǔ)存的勢能,產(chǎn)生室性吸力,是心臟完成心室快速充盈的關(guān)鍵[20]。左室縱向收縮功能是心臟泵功能的重要組成部分,收縮期縱向心肌做功占LVEF的70%[21]。本研究顯示PCOS-IR患者左室各節(jié)段LS及GLS減低,提示在LVEF正常情況下,左室局部及整體心肌縱向收縮功能下降,與Erdoan等[8]及Demirelli等[22]研究結(jié)果一致。Erdoan等[8]認(rèn)為PCOS患者大動(dòng)脈僵硬度上升可導(dǎo)致左室后負(fù)荷增加,破壞縱向心肌纖維結(jié)構(gòu),導(dǎo)致左室局部心肌縱向收縮功能下降。本研究結(jié)果顯示,GLS與FINS、WHR、LDL-C呈負(fù)相關(guān)(r < 0,P < 0.05)。FINS、WHR、LDL-C均為心血管危險(xiǎn)因子,導(dǎo)致PCOS患者左室心肌缺血、纖維化,心內(nèi)膜下縱行心肌與中層及心外膜下心肌比較,對(duì)缺血更為敏感[23],因此縱向心肌收縮功能降低。

        綜上所述,PCOS-IR患者在LVEF正常情況下可出現(xiàn)早期縱向收縮功能下降。CMQ技術(shù)可早期檢測出PCOS-IR患者左心室縱向運(yùn)動(dòng)異常,為臨床及時(shí)干預(yù)治療提供幫助。

        [參考文獻(xiàn)]

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        [2] Hart R,Hickey M,F(xiàn)ranks S. Definitions,prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome [J]. Best Pract Res Clin Obstet Gynaecol,2004,18(5):671-683.

        [3] Dahlgren E,Janson PO,Johansson S,et al. Polycystic ovary syndrome and risk for myocardial infarction:Evaluated from a risk factor model based on a prospective population study of women [J]. Acta Obstet Gynecol Scand,1992, 71(8):599-604.

        [4] The Rotterdam ESHRE/ASRM-sponsored PCOS consensus workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS) [J]. Hum Reprod,2004,19(1):41-47.

        [5] 李昕,林金芳.肥胖型多囊卵巢綜合征患者臨床及內(nèi)分泌代謝特征的研究[J].中華醫(yī)學(xué)雜志,2005,85(46):3266-3271.

        [6] Birdsall MA,F(xiàn)arquhar CM,White HD. Association between polycystic ovaries and extent of coronary artery disease in women having cardiac catheterization [J]. Ann Inter Med,1997,126(1):32-35.

        [7] Dunaif A,Segal KR,F(xiàn)utterweit W,et al. Profound peripheral insulin resistance,independent of obesity,in polycystic ovary syndrome [J]. Diabetes,1989,38(9):1165.

        [8] Erdoan E,Akkaya M,Bacaks?覦z A,et al. Subclinical left ventricular dysfunction in women with polycystic ovary syndrome:an observational study [J]. Anadolu Kardiyol Derg,2013,13(8):784-790.

        [9] Prelevic G M,Beljic T,Balintperic L,et al. Cardiac flow velocity in women with the polycystic ovary syndrome [J]. Clin Endocrinol,1995,43(6):677-681.

        [10] Paradisi G,Steinberg HO,Hempfling A,et al. Polycystic ovary syndrome is associated with endothelial dysfunction [J]. Circulation,2001,103(10):1410-1405.

        [11] Birdsall MA,F(xiàn)arquhar CM,White HD. Association between polycystic ovaries and extent of coronary artery disease in women having cardiac catheterization [J]. Ann Inter Med,1997,126(1):32-35.

        [12] Watts GF,Marwick TH. Ventricular dysfunction in early diabetic heart disease: Detection,mechanisms and significance [J]. Clin Sci(Lond),2003,105(5):537-540.

        [13] Kelly CC,Lyall H,Petrie JR,et al. Low grade chronic inflammation in women with polycystic ovarian syndrome [J]. J Clin Endocrinol Metab,2001,86(6):2453-2455.

        [14] Paradisi G,Steinberg HO,Hempfling A,et al. Polycystic ovary syndrome is associated with endothelial dysfunction [J]. Circulation,2001,103(10):1410-1405.

        [15] Dunaif A. Insulin resistance and the polycystic ovary syndrome:mechanism and implications for pathogenesis [J]. Endocrine Reviews,1997,18(6):774.

        [16] Tlra MB,Yal?觭?覦n R,Noyan V,et al. Alterations in cardiac flow parameters in patients with polycystic ovarian syndrome [J]. Hum Reprod,1999,14:1949-19452.

        [17] Jung B,Odening KE,Dall'Armellina E,et al. A quantitative comparison of regional myocardial motion in mice,rabbits and humans using in-vivo phase contrast CMR [J]. J Cardiovasc Magn Reson,2012,14(1):87.

        [18] Carlsson M,Ugander M,Heiberg E,et al. The quantitative relationship between longitudinal and radial function in left,right,and total heart pumping in humans [J]. Am J Physiol Heart Circ Physiol,2007,293(1):H636.

        [19] Henein MY,Gibson DG. Normal long axis function [J]. Heart,1999,81(2):111.

        [20] Riordan MM,Kovács SJ. Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole:model-based prediction with in vivo validation [J]. Am J Physiol Heart Circ Physiol,2006,291(3):H1210-H1215.

        [21] Brecker SJ. The importance of long axis ventricular function [J]. Heart,2000,84(6):577-579.

        [22] Demirelli S,Deirmenci H,Ermi E,et al. OP-174 the importance of speckle tracking echocardiography in the early detection of left ventricular dysfunction in patients with polycystic ovary syndrome [J]. Am J Cardiol,2015, 115(4):S77-S78.

        [23] Henein MY,Gibson DG. Long axis function in disease [J]. Heart,1999,81(3):229-231.

        (收稿日期:2018-02-25 本文編輯:蘇 暢)

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